Practicals Term I (+BP Prac) Flashcards
Gram +ve bacteria
- have thick peptidoglycan cell walls
- stain purple/blue
- like dry environments
Gram +ve cocci on Gram stain suggest
normal flora
Gram -ve bacteria
- have thin peptidoglycan cell walls and an outer membrane
- do not stain (ie pink or red)
- like moist environments
Gram +ve clusters are
Staphylococci
Gram +ve chains are
Streptococci
Green pus is likely caused by
Pseudomonas aeruginosa
Sulphur granules in pus indicate
Actinomyces israelii
Pus with an offensive odour is likely caused by
anaerobes
Thick, yellow pus is likely caused by
Staphylococcus aureus, etc.
Genetics account for what percent of BP variation in the population?
40%
What happens to systolic BP on sitting??
drops slightly; then restored (but not to lying pressure)
What happens to SV on sitting from lying?
- decreases
- perceived as a slight drop in BP by baroreceptors in carotids and aorta as decreased stretch
- baroreceptors fire to activate medulla to increase SNS tone and decreased PNS tone
- increased SNS and decreased PS increase HR and contractility to restore SV(but not to same level as lying)
What happens to systolic BP on standing from sitting?
initial drop in BP; restored
What happens to SV on standing from sitting?
drops; activates +SNS and -PNS via baroreceptor reflex to increase HR and restore SV
What happens to HR from lying to standing?
increases
What happens to diastolic BP from lying to standing?
decreases
What happens to cardiac output from lying to standing?
decreases
What happens to total peripheral resistance from lying to standing?
decreases
How does the body increase MAP from lying to standing?
by increasing TPR
(inc HR would compromise diastolic filling of coronaries)
Nicotine
increases BP, HR
Caffiene
initially increases blood pressure, long-term effects unknown
What are primary immunodeficiencies?
- result of inherent congenital defects in the components of the immune system or their products
What are secondary immunodeficiencies?
- result from effects of external agents or alterations in other body systems
- more common than primary
- associated with:
- extremes of age
- malnutrition
- anatomic barrier dysfunction (incl medical devices)
- non-infectious diseases (diabetes, tumours/cancer)
- infections (malaria, HIV)
- cytotoxic drugs/irradiation (chemo)
- immunosuppresive drugs
Secondary immunodeficiencies are associated with
- extremes of age
- malnutrition
- anatomic barrier dysfunction (incl medical devices)
- non-infectious diseases (diabetes, tumours/cancer)
- infections (malaria, HIV)
- cytotoxic drugs/irradiation (chemo)
- immunosuppresive drugs
Recessive gene defects that cause primary immunodeficiencies include
- defects in development of primary lymphoid tissue (thymus, spleen)
- defects in T cell development
- MHC Class I or II deficiency
- defects in B cell development and selected antibody deficiencies
- phagocyte deficiencies
- complement pathway deficiencies
What blood specimens are collected for immunodeficiency diagnosis?
- blood - anticoagulant:
- # s and function of immune cells
- blood - plain tube:
- clots; for complement and antibody estimations
What is the order of isotype switching?
IgM > IgG > IgE > IgA
How is blood analysed for populations of lymphocytes?
flow cytometry using anti-T (anti-CD3) and anti-B (anti-CD19) cell antibodies as markers
How are lymphocytes analysed in the blood?
- flow cytometry for populations using anti-T (anti-CD3) and anti-B (anti-CD19) cell antibodies
- antibody isotype analysis (IgG, IgM, IgE, IgA)
- specific antibody analysis (tetanus, blood groups)
- t-cell proliferation tests
- flow cytometry of CD40L expression on activated lymphocytes
How is B-cell function analysed?
presence of antibodies made against immunisation antigens and blood group antigens
If B cell populations are normal but isotype switching is not occurring, where is the immunodeficiency?
T-cells; required for isotype switching
How is T-cell function analysed?
- inducing T-cell proliferation by reacting them with anti-T/anti-CD3 antibodies
- proliferation requires CD25 receptor for IL-2
- expression of CD40L using flow cytometry on activated T cells
CD40L is on
T-cells
What is the function of CD40L?
- required for activating B-cells
- CD40L on T-cells binds to CD40 on B-cells to activate them
- necessary for isotype switching of B cells
- deficiency can cause hyper IgM (isotype cannot switch to IgG)
- activates macrophages
- deficiency means lack of inflammatory cytokine production (afebrile in infection), and defective respiratory burst
- deficiency can also result in:
- poor memory B cell production
- inefficient induction of cyotoxic T-cells
The gene for CD40L is on which chromosome?
X; tf deficiency is x-linked
What is affinity maturation?
the process by which B cells produce antibodies with increased affinity for antigen during the course of an immune response
Monocyte function can be analysed by
- assessing production of TNFa in response to stimulation by IFNy
- TFNa stimulates granuloma formation, macrophage differentiation into giant cells etc.
- tf deficiency in IFNy or IFNyR1 on macrophages results in decreased TNFa production and no granuloma formation where there should be (eg mycobacterium infections)
- flow cytometric analysis for the expression of IFNyR1 (receptor) on monocytes
IFNy is produced by
activated CD4 T cells (particularly Th1)
CD8 T-cells
NK cells
IFNy activates
macrophages
What organisms are common in complicated UTI?
- proteus
- klebsiella
- enterococci
- pseudomonas
Complicated UTIs are associated with
- anatomical abnormalities (including medical devices)
- metabolic abnormalities (pregnancy, diabetes)
- immunocompromise
- unusual pathogens (yeasts)
What bacteria cause UTIs?
- E coli (70-95%)
- Staph saprophyticus (10-20% in sexually active females)
- Proteus (GIT flora)
- Klebsiella (GIT flora)
- Enterococci (GIT flora)
- Pseudomonas (environmental)
What laboratory investigations are undertaken for suspected UTI?
- dip-stick for RBCs, leukocyte exterase, nitrites, protein
- pyuria (pus) measured by counting WBC; >10^4-10^5/mL is abnormal
- casts and crystals (microscopy)
- culture; >10^8/L (>10^5/mL) organisms of a single type in MSU is significant, any grwoth from SPA is significant
What is an abnormal WBC count in urinalysis?
>10^4-10^5/mL
What culture count is significant in UTI?
>10^8/L (>10^5/mL)
What count of RBCs in urine is abnormal?
>2000/mL
Presence of RBC casts on urinalysis indicates
bleeding in the kidney
What media are used in urinalysis?
- HBA (aerobic)
- MAC (aerobic)
- CLED (aerobic)
- Lowenstein-Jensen if renal TB suspected
- Selenite broth if suspected Salmonella Typhi carrier
Bactaeremia
- bacteria in blood
- transient (not uncommon), intermittent, or continuous
- not necessarily associated with clinical features
- requires a mode of entry
Septicaemia
- bacteraemia causing symptoms
- fever, increased CO and RR, changes to body systems/perfusion of organs
- serious
- systemic - sepsis or septic shock
Sepsis
- septicaemia infection
- fever or hypothermia
- tachypnoea or tachycardia
- high or low white cell counts
Septic shock
- severe sepsis
- potentially fatal drop in BP
Bacteria and septicaemia result from
- infection
- massive traua
- inflammatory disease
Systemic inflammatory response syndrome
two or more of:
- temperature >38C or <36C
- resp rate >20/min
- HR >90/min
- WBC >12x10^9/L or <4x10^9/L or >10% immature cells
What are the common gram positive causes of septicaemia?
- staph aureus
- strep pyogenes
- staph epidermidis
- viridans strep
- strep pneumoniae
- enterococcus spp
What are common gram negative causes of septicaemia?
- E. coli
- pseudomonas aurigenosa (environmental)
- klebsiella
- enterobacter spp
- nisseria meningitidis
What are other common causes of septicaemia?
- Candida
- rickettsiae
What are some of the risk factors for septicaemia?
- impaired immunity
- breached integument, neutropenia
- hospitalization
- indwelling (bladder) catheterization
- overseas travel
- occupational
- contact with animals, contaminated food, water
- infection by a virulent pathogen
Sources of septicaemia bacteria are
- skin
- URT
- genito-urinary tract
- GI/biliary tract
GPC are either
staph or strep
Staph is catalase
+ve
Strep is catalase
negative
(as is enterococci)
Staph aureus is coagulase
+ve
Coagulase negative staph are likely
epidermidis (susceptible to novobiocin)
saprophyticius (resisitant to novobiocin)
URTIs are commonly caused by
viruses
sore throat is predominaly
viral infection
sinusitis is predominantly
bacterial infection (often post-viral)
otitis media is often
bacterial infection
LRTIs include
- croup (laryngotracheobronchitis)
- whooping cough
- bronchiolitis
- bronchitis (acute and acute exacerbation of chronic)
- pneumonia
What number of microorganisms in sputum suggest infection?
>10^7/mL
especially of one type
Small numbers of small pink colonies on MAC suggest
growth of normal microbiota (eg e. coli)
How do conjugate vaccines work?
- polysaccharide of capsule conjugated to protein = antigen
- protein antigen presented by APCs to T cells activates them to express CD40L
- polysaccharide antigen recognized by Ig on B cells internalized the conjugate
- peptide portion presented on MHC class II of B cell
- activated T cell binds MHC class II peptide on B cell, CD40 on B cell ligates CD40L
- induces isotype switching, affinity maturation, memory cell secretion
- polysacch on its own cannot activate T cells; can activate some (CD5) B cells (T-indep) but regardless only get IgM and no secondary immune response
- tf peptide conjugate is vital to generating isotype switch and secondary immune response
What is haemolytic uremic syndrome?
- haemolytic anaemia +
- acute kidney failure (uremia) +
- low platelet count (thrombocytopoenia)
